Habitat use in irrigation channels by the golden venus chub (Hemigrammocypris rasborella) at different growth stages.

Ecological information on the golden venus chub (Hemigrammocypris rasborella Fowler, 1910) was collected during field surveys and used to analyze habitat use by this species at each growth stage. Surveys were conducted every month for approximately 2 years In an irrigation ditch near the Ushizu River, Kyushu Island, Japan. Based on the characteristic nuptial coloration of males, it was estimated that H. rasborella spawns between spring and summer. Size measurements of 2697 individuals indicated two size classes. The population of age class 1 decreased rapidly after the spawning period. On the basis of growth patterns, the life cycle of H. rasborella was classified into three stages: the growth stage (GS) of age class 0 fish from August to November, the no-growth stage (NGS) of age class 0 fish from December to March, and the growing and spawning stage (GSS) of age class 0 and 1 fish from April to August. Habitat use by GS, NGS, and GSS fish was analyzed with a stepwise multiple linear regression. The average number of fish was negatively correlated with the presence of a concrete revetment in the GS; positively and negatively correlated with minimum water depth and submerged plants, respectively, in the NGS; and positively correlated with maximum water temperature in the GSS. These results suggest that maintenance of the water level in the fallow season and not using concrete revetments are essential for the conservation of this species under the present conditions in Japanese rice fields.

CD1d-mediated stimulation of natural killer T cells selectively activates hepatic natural killer cells to eliminate experimentally disseminated hepatoma cells in murine liver.

Since hepatocellular carcinomas (HCCs) develop from transformed hepatocytes, sometimes in a multicentrical manner, immunological deletion of such small intrahepatic regions should be an important strategy to prevent HCC development. The liver contains abundant innate cell lineages including natural killer (NK) cells and natural killer T (NKT) cells, the latter of which become activated in a CD1d-restricted manner by alpha-galactosylceramide (alpha-GalCer). In our study, we investigated the anti-tumor effect elicited by alpha-GalCer administration against transplanted hepatoma cells in the liver, in comparison with that in extrahepatic sites. alpha-GalCer administration completely suppressed the growth of BNL 1MEA.7R.1 (BNL) hepatoma cells disseminated in the liver of syngeneic BALB/c mouse but had no anti-tumor effect on subcutaneously implanted BNL cells. Hepatic NKT cells became rapidly activated after alpha-GalCer administration compared to splenic NKT cells and then disappeared. Hepatic NK cells substantially increased their population as well as up-regulated their cytotoxic activity against BNL cells, but NK cells in other tissues, including the spleen, blood and lymph node, did not. Anti-asialo GM1 antibody treatment, which depleted NK cells in vivo, resulted in hepatic tumor formation in alpha-GalCer-treated mice, indicating the critical involvement of NK cells in the alpha-GalCer-induced anti-tumor effect in the liver. In conclusion, our study demonstrates clear differences in NK cell activation and anti-tumor effect through stimulation of NKT cells by alpha-GalCer between the liver and extrahepatic tissues. Sequential activation of these innate cell lineages may be an attractive strategy for controlling micro-disseminated hepatoma cells in the liver.

Impaired expression of proteasome subunits and human leukocyte antigens class I in human colon cancer cells.

BACKGROUND AND AIM: The presentation of human leukocyte antigens (HLA) class I requires the coordinated expression of numerous components involved in antigen processing and antigen presentation. Tumor cells may alter the expression of these components to decrease HLA class I expression, allowing them to escape immune surveillance. The aim of this study is to investigate the expressions of these components, including proteasome subunits, and their involvement in the expression of HLA class I in human colon cancer cells. METHODS: Four human colon cancer cell lines, HCT116, SW403, LoVo and DLD-1, were used to examine the expression of HLA class I by flow cytometry. Reverse transcription-polymerase chain reaction was performed to assess the expression of beta2-microglobulin, heavy chains, transporter subunits, immunoproteasomes subunits and proteasome activator 28 (PA28) subunits. RESULTS: Human leukocyte antigen class I was expressed highly in HCT116 and SW403 cells and weakly in LoVo cells, but was not expressed in DLD-1 cells. The DLD-1 cells were deficient in the expression of proteasome subunits including low molecular weight polypeptide proteasome subunit 2 (LMP2), multicatalytic endopeptidase complex-like-1 (MECL-1), PA28alpha and PA28beta, whereas other HLA class I-expressing cell lines expressed all components tested. gamma-Interferon (IFN-gamma) treatment of DLD-1 cells restored the expression of LMP2, MECL-1 and PA28beta, but not the expression of HLA class I. Enforced expression of PA28alpha induced the expression of HLA class I in IFN-gamma-treated DLD-1 cells, but not in untreated DLD-1 cells. CONCLUSION: These results suggest that the impaired expression of proteasome subunits is involved in the loss of HLA class I expression in human colon cancer cells.